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pharm1 S.Horvath > ANS reversal agents > Flashcards

ANS reversal agents Flashcards

1
Q

what converts dopamine to NE

A

dopamine beta hyroxylase

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2
Q

how is norepinephrine metabolized

A

reuptake (70%), the rest metabolized by monamine oxidase (MAO) and catecholomethyltranserase (COMT)

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3
Q

the alpha 1 receptor is ____synaptic

A

post

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4
Q

alpha 1 works in the

A

periphery

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5
Q

alpha 2 receptor is ___synaptic

A

pre

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6
Q

beta 1 receptor is in the

A

heart

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7
Q

beta 2 is in the

A

other smooth muscle

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8
Q

activation of alpha 1 increases

A

intracellular calcium

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9
Q

alpha 1 causes smooth muscle ___ and peripheral vaso___

A

contraction, vasoconstriction

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10
Q

which anticholinergics are tertiary amines

A

atropine and scopolamne

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11
Q

which anticholinergics are quaternary ammonium

A

glycopyrrolate

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12
Q

electrostatic attachment occurs with

A

edrophonium (competitive)

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13
Q

formation of caramyl esters occurs with

A

neo, phyido, physo (competitive)

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14
Q

phosphorylation occurs with

A

organophosphates and echothiophate (non-competitive inhibition)

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15
Q

how do AchE inhibitors work

A

they reversibly inhibit AchE, which indirectly increases the concentration of Ach at the neuromuscular junction. since more ach is present, it is better able to compete for the alpha binding sites on the nicotinic receptor and antagonize the block

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16
Q

neostigmine is ___ potent than pyridostigmine

A

more

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17
Q

50% of ___ is metabolized by the liver

A

neostigmine

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18
Q

which drugs are quaternary amines

A

endro, neo, phyrido

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19
Q

quaternary pass thru BBB?

A

no

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20
Q

tertiary amine pass thru BBB?

A

yes!

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21
Q

which is tertiary amine

A

physostigmine

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22
Q

AchE inhibitors cause ____ side effects

A

parasympathetic

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23
Q

why do AchE inhibitors cause cholinergic side effects

A

because there is more ach at the muscarinic receptor.

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24
Q

cholinergic side effects are

A

diarrhea , urination, miosis, bradycardia, bronchoconstriction, emesis, lacrimation, laxation, salivation

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25
Q

whats the only AchE inhibitor that diffuses across BBB

A

physostigmine

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26
Q

whats the best AchE inhibitor to antagonize a block with 90% twitch suppression

A

neo

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27
Q

which drugs produce reversible inhibition of AcheE by forming a caramel ester complex at the esteratic site… block the enzymes ability to hydrolyze Ache

A

neo and pyrido and pyrido

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28
Q

which enzyme forms a reversible electrostatic attachment

A

edro

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29
Q

neo edro pyrido. which is most potent

A

neo

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30
Q

neo edro pyrido. which is least potent

A

edro

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31
Q

which drugs prolong the duration of succs

A

neo and pyrido

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32
Q

pyrido edro neo . which has fastest onset

A

endro

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33
Q

pyrido edro neo which has slowest onset

A

pyrido

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34
Q

atropine can be mixed with

A

edro

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35
Q

glyco can be mixed with

A

neostigmine

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36
Q

glyco and edro in the same syringe will cause profound

A

bradycardia (same with administering atropine after edro)

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37
Q

Atropine and scopolamine structure

A

tertiary amines, liophillic

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38
Q

glyco structure

A

quaternary ammonium, does not pass thru lipophilic membranes

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39
Q

sugammadex affinity for amino steroids > > >

A

rec>vec>panc

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40
Q

which drug competitive inhibition, electrostatic attachment

A

edro

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41
Q

metabolism of edro and pyrido

A

75% renal, 25% hepatic

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42
Q

metabolism of neo

A

50% renal, 50% hepatic

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43
Q

neostigmine is ___ in infants and children

A

faster

44
Q

which antimuscarinics pass thru BBB

A

atropine and scop

45
Q

roc metabolism

A

primary biliary

46
Q

sugmmadex metabolism

A

excreted unchanged by kidneys

47
Q

SNS stim effect on bronchial smooth muscle

A

relaxation

48
Q

PNS stim effect on bronchial smooth muscle

A

contraction

49
Q

PNS stim effect on gallbladder

A

contraction

50
Q

PNS stim effect on urinary

A

smooth muscle contraction, sphincter relaxation

51
Q

PNS stim on GI tract

A

inc motility, secretion, sphincter relaxation

52
Q

SNS stim on liver

A

glycogenolysis

53
Q

PSN stim on liver

A

glycogen synthesis

54
Q

SNS stim on eye

A

mydriasis

55
Q

pNS stim on eye

A

miosis

56
Q

SNS stim on pancreas

A

dec beta cell secretion

57
Q

down regulation

A

extended exposure to agonists reduces the number, but not their response. results in tachyphylaxis

58
Q

up regulation

A

chronic depletion of catecholamines or use of antagonists increases the number of receptors but not their sensitivity. may account for withdrawal syndrome with BB

59
Q

receptor uncoupling occurs ___, while sequestration occurs ___

A

rapidly, slowly

60
Q

pheochromocytoma

A

renal tumor. uncontrolled release of catecholamines due to an adrenal gland tumor. constant SNS stimulation. pump out epi and norepinephrine constantly.

61
Q

sympathomimetics

A

compounds that resemble catecholamines except that hydroxyl groups are not present in both the 3 and 4 positions of the benzene ring

62
Q

where is epi released from

A

adrenal medulla , triggered by calcium ion influx

63
Q

presynaptic effect we would see with AchE inhibitor?

A

fasciculation at high doses

64
Q

direct effect of anti cholinesterase ?

A

super high dose causes NMB blockade

65
Q

what is the most important determinant of relative potency ?

A

affinity

66
Q

influence of age with neo

A

infants

67
Q

edrophonium and age

A

no change

68
Q

nicotinic effects occur at

A

NM junction and autonomic ganglia

69
Q

muscarinic effects include

A

bradycardia, salivation, bronchoconstriction, miosis, hyperperistalsis, and increased risk of PONV

70
Q

eye effects from anti cholinesterase

A

miosis, inability to focus on near vision, dec IOP

71
Q

pulm effects from anti cholinesterase

A

bronchoconstriction, increased airway resistance

72
Q

how are anti cholinesterase used to tx myasthenia graves?

A

increase ACh at the nmj

73
Q

potency of anti cholinesterase is determined by

A

NMB being antagonized, speed of spontaneous recovery, and depth of NMB when reversal is initiated

74
Q

whats the purpose of an anticholinergic drug

A

blocks the side effects of the muscarinic receptors

75
Q

administer reversal only after twitch height has recovered to

A

> 10%

76
Q

what can prevent you from properly reversing someone?

A

abx, hypothermia, resp acidosis, hypoK, metabolic acidosis

77
Q

physostigmine CNS effects

A

antagonizes adverse CNS effects of certain drugs

78
Q

which drug decreases post-op somnolence after volatile anesthetic and reverses CNS effects of ketamine

A

physo

79
Q

which drug is used for post op analgesia and post op shivering

A

physo

80
Q

which drug is used for diagnosis and management of cv arrhythmias

A

physo

81
Q

most two significant OD muscarinic effects

A

bronchoconstriction and bradycardia

82
Q

OD nicotinic effects

A

skeletal muscle weakness to paralysis and apnea

83
Q

organophsphate anticholinesterases

A

insecticides and nerve agents - rapidly absorbed - highly lipid soluble - irreversible binding

84
Q

what do you give for OD

A

atropine (for antimuscarinic effects) and pralidoxime (acetylcholinesterase reactivator)

85
Q

anticholinergics antagonize the effects of Ach at ____ receptors

A

muscarinic

86
Q

muscarinic receptors are located

A

heart, salivary glands, smooth muscle GI and Gu tracts

87
Q

anticholinergics MOA

A

competitive antagonists. compete with Ach at the cholinergic/muscarinic receptors

88
Q

m1

A

CNS and stomach

89
Q

m2

A

lungs and heart

90
Q

m3

A

CNS , airway, smooth muscle, glandular tissue

91
Q

m4 and m5

A

CNS

92
Q

m3 causes

A

bronchodilation

93
Q

which drug causes mydriasis and cycloplegia

A

glyco

94
Q

which anticholinergic drug causes most sedation

A

scop

95
Q

which anticholinergic has an increased incidence of memory deficits

A

atropine

96
Q

delated arousal in first 30 min after cessation of anestheisa in patients reversed with

A

atropine/neostigmine

97
Q

which anticholinergics cross the placenta

A

atropine and scop

98
Q

which is the best antisialogogue

A

scop > glco > atropine

99
Q

which has a longer DOA - scop or glyco

A

glyco

100
Q

how does atropine treat intra op bradycardia

A

blocks the effects of ACh on the SA node

101
Q

overdose symptoms of anticholinergics

A

anti-rest and digest. dry mouth, increased temp, dry and flushed skin skeletal weakness, orthostatic hypotension, fatal events

102
Q

treatment for OD of anti-cholinergic

A

physo - may need to repeat dose since it Is metabolized rapidly

103
Q

sugar has a ___ center and ____ exterior

A

hydrophobic, hydrophilic

104
Q

sugga is not recommended for use in

A

severe renal impairment

105
Q

use secondary contraception for ___ post suggamedex

A

one week

pharm1 S.Horvath (18 decks)

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